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Nucleic Acids Research 2006 34(4):1216-1223; doi:10.1093/nar/gkl014
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Published online 25 February 2006

© The Author 2006. Published by Oxford University Press. All rights reserved
The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that: the original authorship is properly and fully attributed; the Journal and Oxford University Press are attributed as the original place of publication with the correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions{at}oxfordjournals.org

Article

Krüppel-like factor 5 is an important mediator for lipopolysaccharide-induced proinflammatory response in intestinal epithelial cells

Sengthong Chanchevalap1, Mandayam O. Nandan1, Beth B. McConnell1, Laetitia Charrier1, Didier Merlin1, Jonathan P. Katz3 and Vincent W. Yang1,2,*

1Division of Digestive Diseases, Department of Medicine, Emory University School of Medicine Atlanta, GA, USA 2Department of Hematology and Oncology, Winship Cancer Institute, Emory University School of Medicine Atlanta, GA, USA 3Division of Gastroenterology, Department of Medicine, University of Pennsylvania School of Medicine Philadelphia, PA, USA

*To whom correspondence should be addressed. Tel: +1 404 727 5638; Fax: +1 404 727 5767; Email: vyang{at}emory.edu

Received January 3, 2006. Revised February 1, 2006. Accepted February 13, 2006.

Lipopolysaccharide (LPS) is a bacterially-derived endotoxin that elicits a strong proinflammatory response in intestinal epithelial cells. It is well established that LPS activates this response through NF-{kappa}B. In addition, LPS signals through the mitogen-activated protein kinase (MAPK) pathway. We previously demonstrated that the Krüppel-like factor 5 [KLF5; also known as intestine-enriched Krüppel-like factor (IKLF)] is activated by the MAPK. In the current study, we examined whether KLF5 mediates the signaling cascade elicited by LPS. Treatment of the intestinal epithelial cell line, IEC6, with LPS resulted in a dose- and time-dependent increase in KLF5 messenger RNA (mRNA) and protein levels. Concurrently, mRNA levels of the p50 and p65 subunits of NF-{kappa}B were increased by LPS treatment. Pretreatment with the MAPK inhibitor, U0126, or the LPS antagonist, polymyxin B, resulted in an attenuation of KLF5, p50 and p65 NF-{kappa}B subunit mRNA levels from LPS treatment. Importantly, suppression of KLF5 by small interfering RNA (siRNA) resulted in a reduction in p50 and p65 subunit mRNA levels and NF-{kappa}B DNA binding activity in response to LPS. LPS treatment also led to an increase in secretion of TNF-{alpha} and IL-6 from IEC6, both of which were reduced by siRNA inhibition of KLF5. In addition, intercellular adhesion molecule-1 (ICAM-1) levels were increased in LPS-treated IEC6 cells and this increase was associated with increased adhesion of Jurkat lymphocytes to IEC6. The induction of ICAM-1 expression and T cell adhesion to IEC6 by LPS were both abrogated by siRNA inhibition of KLF5. These results indicate that KLF5 is an important mediator for the proinflammatory response elicited by LPS in intestinal epithelial cells.


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